Retinal vein occlusion (RVO) is the second most common retinal vascular disorder after diabetic retinopathy. RVOs are divided into central (CRVO), hemi (HRVO), and branch retinal vein occlusions (BRVO). A BRVO is an occlusion of the central retinal vein at the secondary branches or further downstream, resulting in retinal hemorrhages, retinal nonperfusion, and possible subsequent macular edema. Ultimately, there is vision loss due to the nonperfused retina causing visual field defects, or loss of vision results from secondary macular edema.

BRVOs are further classified into ischemic (nonperfused) or nonischemic (perfused). An ischemic BRVO is defined as more than 5 disc diameters of nonperfusion on fluorescein angiography (FA). The ischemic variety portends a poorer prognosis.

A 2010 international meta-analysis by Rogers et al estimated the prevalence of any RVO to be 0.52%, BRVO 0.442%, and CRVO 0.08%. There was no association with sex, but BRVOs were associated with ethnicity with 0.282% of cases occurring in patients of Northern European descent, 0.353% in patients of African descent, 0.498% in patients of Asian descent, and 0.598% in patients of Hispanic descent.

A BRVO is painless and can cause symptomatic decreased vision or may in fact be asymptomatic. Vein occlusion occurs suddenly with resultant localized retinal hemorrhages and exudation. These occur most frequently in the superotemporal quadrant of the retina. With time, retinal neovascularization may occur due to the increased vascular-endothelial growth-factor (VEGF) drive with resultant vitreous hemorrhage and/or neovascular glaucoma. Macular edema, occurring in 90% of BRVO cases, is the main cause of vision loss and is a result of increased inflammatory and VEGF activity.

Risk factors for BRVOs include increased age, race, hypertension, hyperlipidemia, increased body mass index, and glaucoma. Interestingly, while diabetes mellitus is a risk factor for a CRVO, it has not been found to be a risk factor for a BRVO. Hypercoagulable disorders such as hyperhomocysteinemia may also predispose a patient to retinal vein occlusion.

The pathogenesis of a BRVO is multi-factorial and not completely understood. Possible mechanisms include mechanical compression of vessel walls, hypercoagulability, and arteriosclerotic changes.

Possible treatments for BRVOs include laser photocoagulation and anti-VEGF intravitreal injections.

BRVO cases have a good visual prognosis with 50%-60% of patients having a final visual acuity of 20/40 or better even without treatment.